Stimulation of bumetanide-sensitive K+ transport in Swiss 3T3 fibroblasts by serum and mitogenic hormones.

Stimulation of bumetanide-sensitive K+ transport in Swiss 3T3 fibroblasts by serum and mitogenic hormones.
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血清和促有丝分裂激素刺激瑞士 3T3 成纤维细胞中布美他尼敏感的 K 转运。

DOI:
10.1002/jcp.1041230216
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发表时间:
1985
影响因子:
5.6
通讯作者:
Adelberg,EA
Adelberg,EA
中科院分区:
生物学2区
文献类型:
--
作者:
Amsler,K;Donahue,JJ;Slayman,CW;Adelberg,EA

文献摘要

相似文献

快速生长的Swiss 3T3成纤维细胞具有布美他胺敏感的K+转运系统,该系统依赖于Na+和Cl−离子;也存在较小的对K+输运不敏感的布美他胺成分。在不改变培养基的情况下,在8-11天孵育后进入静止状态的细胞中,布美他胺的转运敏感性降低了63%;布美他胺不敏感率没有变化。从摄取培养基中去除透析的胎牛血清导致快速生长细胞(减少33%)和静止细胞(减少68%)对布美他尼敏感的摄取大幅减少,但对布美他尼不敏感的摄取没有影响。在刺激布美他尼敏感摄取方面,胰岛素几乎与透析后的胎牛血清一样有效;胰岛素在2.5 μg/ml时刺激作用最大。胰岛素、表皮生长因子和精氨酸-抗利尿素联合使用在刺激静止细胞对布美他尼敏感的K+摄取和3h -胸苷结合方面最有效;然而,布美他尼不会干扰激素对DNA合成的刺激。因此,布美他胺敏感的K+转运系统对于这种刺激的发生并不是必需的。此外,刺激DNA合成水平的激素浓度不会提高细胞内K+浓度。我们得出结论,布美他尼敏感的K+转运途径受到血清和有丝分裂激素的调节,但在这些因素对DNA合成的刺激中不起作用。
Rapidly growing Swiss 3T3 fibroblasts possess a bumetanide‐sensitive K+transport system that is dependent on both Na+and Cl−ions; a smaller bumetanide‐insensitive component of K+transport is also present. In cells brought to the quiescent state by 8–11 days of incubation without a medium change, the bumetanide‐sensitive rate of transport was reduced by 63%; the bumetanide‐insensitive rate did not change. Removal of dialyzed fetal calf serum from the uptake medium resulted in a substantial reduction in bumetanide‐sensitive uptake in both rapidly growing cells (33% reduction) and quiescent cells (68% reduction) but had no effect on bumetanide‐insensitive uptake. Insulin was almost as effective as dialyzed fetal calf serum in stimulating bumetanide‐sensitive uptake; insulin was maximally stimulatory at 2.5 μg/ml. The combination of insulin, epidermal growth factor, and arginine‐vasopressin was maximally effective in stimulating both bumetanide‐sensitive K+uptake and3H‐thymidine incorporation in quiescent cells; bumetanide, however, did not interfere with the hormonal stimulation of DNA synthesis. Thus, the bumetanide‐sensitive K+transport system is not necessary for such stimulation to occur. Furthermore, concentrations of hormones which stimulated significant levels of DNA synthesis produced no elevation in the intracellular concentration of K+. We conclude that the bumetanide‐sensitive pathway of K+transport is modulated by serum and by mitogenic hormones, but does not play a role in the stimulation of DNA synthesis by these factors.